Neuropsychology -- dementia and affective disorders

Robbins, Trevor W.; Elliott, Rebecca; Sahakian, Barbara J.

doi:10.1093/oxfordjournals.bmb.a011572

Cited by 32 publications

(13 citation statements)

References 43 publications

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“…Striatal pathophysiology may compromise function in cortico-striatal loops that feed back to the orbital, cingulate and medial prefrontal cortex (Alexander et al 1986). It has been suggested that depression is associated with disrupted function within frontostriatal loops (Robbins et al 1992) and our functional imaging studies suggest that the prefrontal expression of this abnormality may depend on the specific cognitive requirements imposed on patients.…”

Section: Discussionmentioning

confidence: 68%

Abnormal neural response to feedback on planning and guessing tasks in patients with unipolar depression

et al. 1998

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Background. It has been suggested that patients with unipolar depression show abnormal responses to negative feedback in the performance of cognitive tasks. Positron emission tomography (PET) has previously identified blood flow abnormalities in depressed patients during cognitive performance. We have also used PET to identify regions where there is differential neural response to performance feedback in normal volunteers. In this study we aimed to test the hypothesis that blood flow in these regions, the medial caudate and ventromedial prefrontal cortex, would be abnormal in depressed patients. Methods. Six patients with unipolar depression and six matched controls were scanned using PET while performing cognitive tasks in the presence and absence of feedback. Results. Compared with controls, depressed patients failed to show significant activation in the medial caudate and ventromedial orbitofrontal cortex. Blood flow was lower and a differential response, observed in normals, under different task and feedback conditions was not seen in the patients. Discussion. The findings suggest that the behavioural response to feedback in depressed patients is associated with an abnormal neural response within the medial caudate and ventromedial orbitofrontal cortex, regions implicated in reward mechanisms. We argue that the observed abnormalities may depend on a combination of psychological factors, with both cognitive and emotive components.

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Section: Discussionmentioning

confidence: 68%

Abnormal neural response to feedback on planning and guessing tasks in patients with unipolar depression

et al. 1998

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“…Finally, an association between depression and prefrontal abnormalities has been demonstrated in neuroimaging studies conducted in depressed patients, with suggested disruptions of frontostriatal (99) and corticolimbic (100) networks. Results of these studies revealed resting abnormalities in the dorsolateral, ventrolateral, and medial aspects of the prefrontal cortex and the anterior cingulate, blunted responses in the anterior cingulate and medial prefrontal cortex to behavioral and pharmacological challenges, and abnormalities localized to the orbitofrontal cortex (100,101).…”

Section: Dysthymiamentioning

confidence: 95%

Drug Addiction and Its Underlying Neurobiological Basis: Neuroimaging Evidence for the Involvement of the Frontal Cortex

Goldstein

Volkow²

2002

AJP

2,372

102

1,717

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Objective-Studies of the neurobiological processes underlying drug addiction primarily have focused on limbic subcortical structures. Here the authors evaluated the role of frontal cortical structures in drug addiction.Method-An integrated model of drug addiction that encompasses intoxication, bingeing, withdrawal, and craving is proposed. This model and findings from neuroimaging studies on the behavioral, cognitive, and emotional processes that are at the core of drug addiction were used to analyze the involvement of frontal structures in drug addiction. Results-The orbitofrontal cortex and the anterior cingulate gyrus, which are regions neuroanatomically connected with limbic structures, are the frontal cortical areas most frequently implicated in drug addiction. They are activated in addicted subjects during intoxication, craving, and bingeing, and they are deactivated during withdrawal. These regions are also involved in higherorder cognitive and motivational functions, such as the ability to track, update, and modulate the salience of a reinforcer as a function of context and expectation and the ability to control and inhibit prepotent responses.Conclusions-These results imply that addiction connotes cortically regulated cognitive and emotional processes, which result in the overvaluing of drug reinforcers, the undervaluing of alternative reinforcers, and deficits in inhibitory control for drug responses. These changes in addiction, which the authors call I-RISA (impaired response inhibition and salience attribution), expand the traditional concepts of drug dependence that emphasize limbic-regulated responses to pleasure and reward.Addiction is a complex disease process of the brain that results from recurring drug intoxication and is modulated by genetic, developmental, experiential, and environmental factors. The neurobiological changes that accompany drug addiction are not well understood. While until recently it was believed that addiction predominantly involved reward processes mediated by limbic circuits (see, for example, the reward deficiency syndrome [1]), results from recent neuroimaging studies have implicated additional brain areas, especially the frontal cortex. Here we summarize the findings from these neuroimaging studies and incorporate them with pertinent results from preclinical studies in suggesting a basis for an integrated model of drug addiction.Most imaging studies have concentrated on the involvement of dopamine in the process of drug addiction because the ability of drugs of abuse to increase brain dopamine concentration in limbic brain regions is considered crucial for their reinforcing effects (2,3). However, the Address reprint requests to Dr. Goldstein, Brookhaven National Laboratory, Medical Research, Bldg. 490, 30 Bell Ave, Upton, NY 11973; rgoldstein@bnl.gov (e-mail NIH-PA Author ManuscriptNIH-PA Author Manuscript NIH-PA Author Manuscript increase in dopamine per se is insufficient to account for the process of addiction, since drugs of abuse increase dopamine in n...

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“…Such behavioral aberrations, for example, are common in depressive states in which patients' reactions to negative feedback are often exaggerated, whereas positive events fail to adequately reinforce behavior (Beats et al, 1996;Elliott et al, 1996;Henriques et al, 1994;Hughes et al, 1985;Murphy et al, 2003;Robbins et al, 1996;Steffens et al, 2001). The abnormal response to negative feedback showed by depressive patients can be seen as part of a larger motivational deficit and is considered to be an important link between emotional and cognitive disturbances in depression (Elliott et al, 1997).…”

Section: Introductionmentioning

confidence: 99%

Serotonin Modulates Sensitivity to Reward and Negative Feedback in a Probabilistic Reversal Learning Task in Rats

Bari

Theobald

Caprioli

et al. 2010

Neuropsychopharmacol

298

338

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Depressed patients show cognitive deficits that may depend on an abnormal reaction to positive and negative feedback. The precise neurochemical mechanisms responsible for such cognitive abnormalities have not yet been clearly characterized, although serotoninergic dysfunction is frequently associated with depression. In three experiments described here, we investigated the effects of different manipulations of central serotonin (5-hydroxytryptamine, 5-HT) levels in rats performing a probabilistic reversal learning task that measures response to feedback. Increasing or decreasing 5-HT tone differentially affected behavioral indices of cognitive flexibility (reversals completed), reward sensitivity (win-stay), and reaction to negative feedback (lose-shift). A single low dose of the selective serotonin reuptake inhibitor citalopram (1 mg/kg) resulted in fewer reversals completed and increased lose-shift behavior. By contrast, a single higher dose of citalopram (10 mg/kg) exerted the opposite effect on both measures. Repeated (5 mg/kg, daily, 7 days) and subchronic (10 mg/kg, b.i.d., 5 days) administration of citalopram increased the number of reversals completed by the animals and increased the frequency of win-stay behavior, whereas global 5-HT depletion had the opposite effect on both indices. These results show that boosting 5-HT neurotransmission decreases negative feedback sensitivity and increases reward (positive feedback) sensitivity, whereas reducing it has the opposite effect. However, these effects depend on the nature of the manipulation used: acute manipulations of the 5-HT system modulate negative feedback sensitivity, whereas long-lasting treatments specifically affect reward sensitivity. These results parallel some of the findings in humans on effects of 5-HT manipulations and are relevant to hypotheses of altered response to feedback in depression.

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Neuropsychology -- dementia and affective disorders

Cited by 32 publications

References 43 publications

Abnormal neural response to feedback on planning and guessing tasks in patients with unipolar depression

Abnormal neural response to feedback on planning and guessing tasks in patients with unipolar depression

Drug Addiction and Its Underlying Neurobiological Basis: Neuroimaging Evidence for the Involvement of the Frontal Cortex

Serotonin Modulates Sensitivity to Reward and Negative Feedback in a Probabilistic Reversal Learning Task in Rats

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